ArticleOncoimmunology2026
Pleiotropic effects of BET inhibition broadly boost tumor immunogenicity to CD8
Article in Oncoimmunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BET inhibitors (BETi) have shown potential to augment tumor immunogenicity in melanoma. However, conflicting evidence exists regarding their precise mechanism of action, and their overall impact on melanoma immunogenicity and antitumoral T cell responses remains unclear. To address this, human melanoma cell lines treated with JQ1 and/or IFNγ were investigated for gene and protein expression changes in key pathways governing immunogenicity and cocultured with autologous tumor-infiltrating lymphocytes (TIL) with known antigen-specificity. JQ1-induced proteome-wide alterations were examined using mass spectrometry-based cellular thermal shift assay (MS-CETSA), which revealed that JQ1 broadly impacts melanoma immunogenicity by regulating IFN signaling, antigen processing and presentation, and innate immune signaling pathways. More specifically, JQ1 enhanced JAK1/STAT1 signaling and upregulated components of the HLA class I (HLA-I) antigen processing and presentation machinery (APM), increased MART-1 expression while concomitantly dampening tumoral expression of PD-L1, IDO1, and HLA class II (HLA-II). Functionally, JQ1 markedly improved tumor recognition by autologous MART-1- and neoantigen-specific CD8
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